The precise ways in which MACs, polyphenols, and PUFAs affect the redox state remain unclear, although the effectiveness of SCFAs as Nrf2 activators suggests their potential role in the antioxidant action of dietary bioactive compounds. This review synthesizes the core mechanisms by which MACs, polyphenols, and PUFAs influence host redox homeostasis, specifically highlighting their capacity to either directly or indirectly activate the Nrf2 pathway. Their probiotic effects, and the role of gut microbiota metabolic/compositional shifts in producing potential Nrf2 ligands (like SCFAs) for host redox balance, are discussed.
Obesity's chronic low-grade inflammatory state directly results in oxidative stress and a pro-inflammatory cascade. The consequences of oxidative stress and inflammation encompass brain atrophy and morphological alterations, culminating in cognitive impairments. Despite the mounting evidence, a cohesive study detailing the combined effect of oxidative stress, inflammation, obesity, and cognitive impairment is absent. Accordingly, this review intends to recapitulate the current importance of oxidative stress and inflammation in causing cognitive decline, based on observations from in vivo studies. Nature, Medline, Ovid, ScienceDirect, and PubMed were systematically searched for publications within the last ten years, encompassing a comprehensive review. Our search uncovered 27 articles requiring further evaluation and a more thorough review. Obesity, characterized by elevated fat storage within adipocytes, is implicated by this research in the genesis of reactive oxygen species and inflammation. This action will trigger oxidative stress, leading to potential changes in brain morphology, a suppression of the natural antioxidant system, the promotion of neuroinflammation, and, ultimately, the demise of neurons. The normal functioning of the brain, including regions crucial for learning and memory, will be compromised. This observation highlights a robust positive correlation between obesity and cognitive impairments. Therefore, this overview details the process by which oxidative stress and inflammation cause memory loss, supported by findings from animal models. This review concludes with potential implications for future therapeutic interventions targeting oxidative stress and inflammatory pathways, thus addressing obesity-induced cognitive decline.
Stevioside, possessing potent antioxidant activity, is a natural sweetener extracted from the Stevia rebaudiana Bertoni plant. Despite this, there is a paucity of information regarding the protective role of this factor in maintaining the health of intestinal epithelial cells subjected to oxidative stress. This research examined the underlying mechanisms through which stevioside protects intestinal porcine epithelial cells (IPEC-J2) from oxidative stress induced by diquat, considering its impact on inflammation, apoptosis, and improvement of antioxidant capacity. Compared to diquat-alone-treated IPEC-J2 cells, a 6-hour stevioside (250µM) pretreatment significantly enhanced cell viability and proliferation, while also preventing the apoptosis induced by 6-hour diquat (1000µM) exposure. The pretreatment with stevioside demonstrably lowered the production of ROS and MDA, and importantly, elevated the activity of T-SOD, catalase (CAT), and glutathione peroxidase (GSH-Px). Subsequently, intestinal barrier function was enhanced, and cell permeability was decreased, owing to a substantial elevation in the expression levels of tight junction proteins such as claudin-1, occludin, and ZO-1. Stevioside, in combination with diquat treatment, significantly reduced the secretion and expression of pro-inflammatory cytokines IL-6, IL-8, and TNF-, and diminished phosphorylation of the key signalling proteins NF-κB, IκB, and ERK1/2. In this study, the effect of stevioside on diquat-induced harm to IPEC-J2 cells was explored. The results showed that stevioside mitigated diquat-stimulated cytotoxicity, inflammation, and apoptosis, maintaining cellular barrier integrity and reducing oxidative stress, by impacting the NF-κB and MAPK signaling pathways.
Reputable experimental investigations show that oxidative stress is the leading cause of the onset and progression of major human health concerns including cardiovascular, neurological, metabolic, and cancer-related ailments. The presence of elevated reactive oxygen species (ROS) and nitrogen species is a factor in the damage observed in proteins, lipids, and DNA, increasing the risk of chronic human degenerative disorders. Current biological and pharmaceutical research efforts are directed toward investigating oxidative stress and its defensive systems, aiming to manage health-related impairments. Therefore, interest in naturally occurring antioxidant compounds, derived from food plants, has markedly increased in recent years, offering the potential to prevent, reverse, or lessen susceptibility to chronic diseases. To address this research objective, this review evaluates the advantages of carotenoids for human health. Naturally occurring in a wide array of fruits and vegetables, carotenoids are bioactive compounds. Scientific investigation has highlighted the diverse biological functions of carotenoids, from their antioxidant and anti-tumor properties to their anti-diabetic, anti-aging, and anti-inflammatory effects. An overview of the most recent advancements in carotenoid biochemistry, highlighting lycopene's properties, and their potential in preventative and therapeutic human health applications is presented in this paper. To improve the research and investigation into carotenoids as potential components of functional health foods and nutraceuticals across the fields of healthy products, cosmetics, medicine, and the chemical industry, this review can act as a starting point.
Alcohol exposure prior to birth can lead to adverse cardiovascular outcomes in the subsequent generation. Epigallocatechin-3-gallate (EGCG) could potentially function as a safeguard, but unfortunately, no data exist regarding its effect on cardiac impairment. Immuno-related genes We examined cardiac changes in mice exposed to alcohol during gestation and the impact of subsequent EGCG treatment on cardiac performance and associated biochemical processes. On gestation days 1–19, C57BL/6J pregnant mice were administered either 15 g/kg/day of ethanol (Mediterranean pattern), 45 g/kg/day of ethanol (binge pattern), or maltodextrin. Subsequent to the delivery, the treatment groups consumed water supplemented with EGCG. Postnatal day sixty marked the time for performing functional echocardiography. A Western blot analysis was performed to characterize heart biomarkers reflecting apoptosis, oxidative stress, and cardiac harm. The Mediterranean alcohol pattern, when administered prenatally to mice, caused an increase in BNP and HIF1, and a decrease in Nrf2 expression. Hepatocyte fraction Binge PAE drinking resulted in a decrease of Bcl-2 protein expression. Both ethanol exposure scenarios showed increases in Troponin I, glutathione peroxidase, and Bax concentrations. Prenatal alcohol exposure's impact on mice involved cardiac dysfunction, which manifested as decreased ejection fraction, a reduced left ventricular posterior wall thickness during diastole, and an elevated Tei index. Restoring the physiological levels of these biomarkers, postnatal EGCG therapy facilitated the improvement of cardiac function. The cardiac damage induced by prenatal alcohol exposure in offspring is shown by these findings to be lessened by postnatal EGCG treatment.
Elevated inflammation and oxidative stress are theorized to be implicated in the pathophysiological characteristics of schizophrenia. We endeavored to determine if incorporating anti-inflammatory and anti-oxidant drug use during pregnancy could potentially prevent the appearance of schizophrenia-related consequences in a gestational rat model of this neurodevelopmental disorder.
Following injection with polyriboinosinic-polyribocytidilic acid (Poly IC) or saline, pregnant Wistar rats underwent subsequent treatment with either N-acetyl cysteine (NAC) or omega-3 polyunsaturated fatty acids (PUFAs) throughout gestation until delivery. Treatment was absent for the control group of rodents. Evaluations of neuroinflammation and anti-oxidant enzyme activity were conducted in the offspring at postnatal days 21, 33, 48, and 90. learn more Behavioral testing at PND 90 was the preliminary step in a multifaceted study, followed by ex vivo MRI analysis and post-mortem neurochemical assessment.
The supplemental treatment facilitated a more expeditious restoration of dam wellbeing. Supplementing adolescent Poly IC offspring with the treatment mitigated the intensification of microglial activity and, to a degree, prevented an impairment in the antioxidant defense system. Adult Poly IC offspring receiving supplemental treatment partially avoided dopamine deficits, accompanied by certain behavioral shifts. By exposing the system to omega-3 PUFAs, lateral ventricle expansion was prevented.
High intake of over-the-counter supplements may be helpful in specifically addressing the inflammatory aspects of schizophrenia's pathophysiology, thus contributing to a decrease in disease severity in later generations.
Over-the-counter supplements, when taken in sufficient quantities, might specifically address the inflammatory processes implicated in schizophrenia's underlying mechanisms, potentially mitigating the severity of the disease in future generations.
The World Health Organization is targeting a cessation of diabetes's growth by 2025, with dietary management being a paramount non-pharmacological preventive method. Bread enriched with resveratrol (RSV), a naturally occurring compound with anti-diabetic effects, becomes a readily available source of this beneficial substance for consumers, seamlessly integrating it into their daily diet. In a live animal model, this study examined the ability of RSV-infused bread to avert the emergence of cardiomyopathy associated with early-stage type 2 diabetes. Sprague-Dawley rats, three weeks old, were divided into four groups: controls receiving plain bread (CB) or RSV bread (CBR), and diabetics receiving plain bread (DB) or RSV bread (DBR).